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Related Experiment Video

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LPCAT3 deficiency Drives phospholipid remodeling and mitochondrial oxidative dysfunction to accelerate MASH-HCC

Gaoxuan Shao1, Chenhao Ye2, Chenceng Sun2

  • 1Institute of Digestive Diseases, Longhua Hospital, China-Canada Center of Research for Digestive Diseases (ccCRDD), Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China; State Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine (Shanghai University of Traditional Chinese Medicine), Shanghai 200032, China; Shanghai Frontier Research Center of Disease and Syndrome Biology of Inflammatory Cancer Transformation, Shanghai 200032, China.

Journal of Advanced Research
|April 8, 2026
PubMed
Summary

Lysophosphatidylcholine acyltransferase 3 (LPCAT3) deficiency worsens metabolic dysfunction-associated steatohepatitis (MASH) and promotes liver cancer by impairing mitochondrial function. Restoring LPCAT3 inhibits MASH-to-HCC progression, highlighting LPCAT3 as a therapeutic target.

Keywords:
Lysophosphatidylcholine acyltransferase 3MASH-HCC progressionMitochondrial dysfunctionPdi–Ero1α pathwayPhospholipid remodeling

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Oncology

Background:

  • Metabolic dysfunction-associated steatohepatitis (MASH) is a severe form of MAFLD that can progress to hepatocellular carcinoma (HCC).
  • Lysophosphatidylcholine acyltransferase 3 (LPCAT3) is crucial for cellular homeostasis, but its role in MASH-to-HCC progression is unknown.

Purpose of the Study:

  • To elucidate the mechanism by which LPCAT3 influences the progression from MASH to HCC.

Main Methods:

  • Examined LPCAT3 expression in human MASH-HCC tissues.
  • Utilized a MASH-HCC mouse model with high-fat, high-cholesterol diet.
  • Performed lipidomics and proteomics analyses.
  • Generated liver-specific LPCAT3 knockout and overexpression (AAV) mouse models.

Main Results:

  • Hepatic LPCAT3 expression was reduced in MASH mice.
  • LPCAT3 deficiency accelerated MASH progression, increasing inflammation and fibrosis, and promoting HCC.
  • LPCAT3 deficiency upregulated Pdi-Ero1α, causing mitochondrial H₂O₂ and Ca²⁺ accumulation and impaired oxidative phosphorylation.
  • Supplementing PC (18:2/18:2) reversed these effects.
  • LPCAT3 overexpression ameliorated mitochondrial dysfunction and inhibited MASH-to-HCC progression.

Conclusions:

  • LPCAT3 deficiency drives Pdi-Ero1α-mediated mitochondrial dysfunction in MASH-associated HCC.
  • LPCAT3 is identified as a potential therapeutic target for MASH-associated HCC.